预约演示
更新于：2026-04-20
Sparsentan
司帕生坦
更新于：2026-04-20
概要
基本信息
药物类型 小分子化药 |
别名 Sparsentan (USAN/INN)、BMS-346567、PS-433540 + [2] |
作用方式 拮抗剂 |
作用机制 AT1R拮抗剂(血管紧张素II-1型受体拮抗剂)、ETA拮抗剂(内皮素A受体拮抗剂) |
在研适应症 |
非在研适应症 |
最高研发阶段批准上市 |
首次获批日期 美国 (2023-02-17), |
最高研发阶段(中国)- |
特殊审评优先审评 (美国)、加速批准 (美国)、孤儿药 (美国)、孤儿药 (欧盟)、孤儿药 (日本)、附条件批准 (欧盟)、孤儿药 (英国)、孤儿药 (澳大利亚) |
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结构/序列
分子式C32H40N4O5S |
InChIKeyWRFHGDPIDHPWIQ-UHFFFAOYSA-N |
CAS号254740-64-2 |
关联
14
项与 司帕生坦 相关的临床试验NCT07224776
Sparsentan for the Treatment of VEGF Signaling Pathway Inhibitor-Associated Proteinuria
NCT07219121
A Multicenter, Open-label Single Arm Study to Evaluate the Safety and Efficacy of Sparsentan in Posttransplant Immunoglobulin A Nephropathy (IgAN) or Focal Segmental Glomerulosclerosis (FSGS) (SPARX)
JPRN-jRCT2051240070
Phase 3, multicenter, open-label, single-arm study to evaluate the efficacy and safety of RE-021 in Japanese patients with IgA nephropathy
100 项与 司帕生坦 相关的临床结果
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100 项与 司帕生坦 相关的转化医学
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100 项与 司帕生坦 相关的专利（医药）
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87
项与 司帕生坦 相关的文献（医药）2026-03-03JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
IgA Nephropathy in Adults
Review
作者: Teh, Jia Wei ; Stoneman, Sinead ; O’Shaughnessy, Michelle Marie
Importance:
IgA nephropathy (IgAN) is a chronic kidney disease involving deposition of IgA-containing immune complexes in the glomerulus, causing glomerular inflammation and scarring. It is the most common immune-mediated glomerular disease worldwide, and affects an estimated 198 887 to 208 184 persons in the US. Up to 50% of patients with IgAN develop kidney failure within 10 years of diagnosis.
Observations:
IgAN typically presents with nephritic syndrome and usually occurs in younger adults, with a mean age at diagnosis of 34 to 45 years. Incidence is highest in East Asia. Approximately 60% of cases are detected incidentally with hematuria or proteinuria on urinalysis. Up to 30% of patients present with episodic visible hematuria, often concomitantly with an upper respiratory or gastrointestinal tract infection (synpharyngitic hematuria). Less common presentations include nephrotic syndrome (<5%) and rapidly progressive glomerulonephritis (<5%). When IgAN is suspected (due to hematuria, proteinuria, or reduced kidney function), initial workup should include quantification of proteinuria and assessment for other causes of nephritic syndrome (eg, lupus nephritis). Adults with suspected IgAN and proteinuria greater than or equal to 0.5 g per day should undergo kidney biopsy. The diagnosis of primary IgAN is based on presence of IgA-dominant immune deposits in the glomerular mesangium after excluding other causes of this histologic appearance, ie, IgA vasculitis, IgA-dominant infection-related glomerulonephritis, and secondary IgAN from diseases such as cirrhosis, inflammatory bowel disease, celiac disease, infection (eg, viral hepatitis), and autoimmune diseases (eg, axial spondyloarthritis). Based on the Kidney Disease: Improving Global Outcomes 2025 clinical practice guideline for the management of IgAN, treatment for patients with proteinuria greater than 0.5 g per day includes behavioral modifications (eg, dietary sodium <2 g/d, smoking cessation, weight control, exercise), antihypertensive medications for goal blood pressure less than 120/70 mm Hg, and therapies to reduce the formation of IgA-containing immune complexes (eg, targeted-release budesonide), decrease glomerular injury (eg, systemic glucocorticoids, iptacopan), and manage existing IgAN-induced nephron loss (eg, renin-angiotensin system inhibitor or dual endothelin angiotensin receptor antagonist [eg, sparsentan] alone or in combination with a sodium-glucose cotransporter 2 inhibitor).
Conclusions and Relevance:
IgAN is the leading cause of immune-mediated glomerular disease worldwide. Patients with suspected IgAN and proteinuria greater than or equal to 0.5 g per day should undergo kidney biopsy to confirm the diagnosis. Treatment of IgAN includes behavioral modifications, blood pressure management, and therapies to decrease formation of IgA-containing immune complexes (eg, targeted-release budesonide), reduce immune complex–mediated glomerular injury (eg, systemic glucocorticoids, iptacopan), and manage IgAN-induced nephron loss (eg, renin-angiotensin system inhibitor, dual endothelin angiotensin receptor antagonist, and sodium-glucose cotransporter 2 inhibitor).
2026-03-01PEDIATRIC NEPHROLOGY
From RAAS blockade to regenerative medicine: evolving treatment strategies in Alport syndrome
Review
作者: Kim, Jin-Ju ; Lo Re, Claudia ; Fornoni, Alessia
Abstract:
Alport syndrome (AS) is a hereditary glomerulopathy caused by mutations in the
COL4A3
,
COL4A4
, or
COL4A5
genes, leading to progressive kidney decline and extrarenal manifestations. Advances in genetic testing have enabled the reclassification of AS into X-linked, autosomal recessive, and autosomal dominant forms, facilitating more accurate diagnosis and risk stratification. While renin-angiotensin-aldosterone system (RAAS) blockade remains the foundation of treatment to delay kidney failure, it does not directly target the underlying molecular pathology. Adjunctive commercially available metabolic modulators, including SGLT2i, mineralocorticoid receptor antagonists, ezetimibe and GLP-1 receptor agonists, may offer additional kidney protection. Ameliorating therapies being tested in Phase II trials include endothelin receptor antagonists (e.g., atrasentan), dual endothelin receptor antagonist and angiotensin II receptor inhibition (e.g., sparsentan) FXR agonists (e.g., vonafexor), inducers of cholesterol efflux (e.g., VAR200 and R3R01), and NOX1/4 inhibitors (e.g., setanaxib), several of which are currently being evaluated in clinical trials. Novel strategies such as exon skipping, gene editing, and nonsense mutation readthrough (e.g., ELX-02) are advancing toward precision medicine approaches as disease modifying agents targeting the genetic cause of AS. Moreover, therapies targeting mitochondrial function, such as mitophagy enhancers, have demonstrated preclinical promise. Stem cell-based approaches are also being explored for their regenerative and anti-fibrotic effects. This review summarizes the current landscape of AS classification and treatment, highlighting both standard interventions and experimental therapies. Emphasis is placed on the molecular mechanisms underlying podocyte injury and fibrosis, recent preclinical findings, and ongoing clinical trials that may shift future therapeutic paradigms.
Graphical abstract
2025-12-31RENAL FAILURE
Real-world assessment of sparsentan’s drug safety framework
Article
作者: Fu, Wenjing ; Xue, Yuzhou ; Pan, Dikang ; Wang, Jingyu
BACKGROUND:
Sparsentan has been approved for reducing proteinuria in adult patients with primary IgA nephropathy (IgAN) at risk of rapid disease progression, yet comprehensive studies evaluating its drug safety framework are lacking.
METHODS:
Adverse event (AE) reports following the market release of sparsentan were collected from the U.S. Food and Drug Administration AE Reporting System. Disproportionate analysis was used to identify previously unrecognized positive novel signals at both the system organ class and preferred term levels. Additionally, analysis on clinical priorities and subgroup analysis were conducted.
RESULTS:
A total of 504 patients with IgAN were included. Two novel system organ classes and 14 novel preferred terms were identified. Hypotension and dizziness were established as moderate clinical priority events. Males had a higher relative risk of nausea, peripheral edema, feeling abnormal, decreased blood pressure, and hypotension, while females were at greater risk for fatigue, pain, increased blood creatinine, dizziness, and somnolence. Among those aged 18-45, the relative risk of experiencing fatigue, pain, and dizziness was higher, individuals aged 45 and older had a higher relative risk of peripheral edema, decreased blood pressure, and hypotension.
CONCLUSIONS:
Based on the available AE reporting data, sparsentan exhibits a favorable safety profile, with no high-priority clinical events identified. Our findings offer valuable insights to optimize the use of sparsentan and understand its potential side effects.
100 项与 司帕生坦 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 局灶性节段性肾小球硬化症 | 美国 | 2026-04-13 | |
| 免疫球蛋白a肾病 | 美国 | 2023-02-17 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 抗中性粒细胞胞质抗体相关性血管炎 | 临床2期 | 英国 | 2022-12-08 | |
| 肾脏疾病 | 临床2期 | 英国 | 2022-12-08 | |
| 肾小球疾病 | 临床2期 | 美国 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 德国 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 意大利 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 荷兰 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 波兰 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 西班牙 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 瑞典 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 英国 | 2021-08-12 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床2期 | 48 | 製鏇襯壓齋襯艱淵獵獵(夢蓋糧鹹夢築鏇膚構積) = 獵鑰遞鬱築衊廠選蓋廠 範製願遞醖窪齋顧觸餘 (範簾餘襯壓醖觸廠衊鏇, 築範範窪選淵觸憲糧夢 ~ 遞醖艱齋醖顧選繭壓觸) 更多 | - | 2025-11-20 | |||
N/A | 22 | 網艱艱衊獵廠製製鹽繭(顧餘積糧餘繭構鹹觸窪) = 製鹹選襯鹹顧鑰簾願壓 構構憲餘夢壓鹹遞齋憲 (獵窪築製壓積夢鹽鬱蓋, 0.2) 更多 | 积极 | 2025-11-08 | |||
N/A | 620 | SGLT2 inhibitors | 齋蓋廠簾齋壓製選鏇範(衊窪範鬱糧廠醖鏇網鏇) = Nephrologists rank FSGS among the top three rare kidney diseases with sizable unmet therapeutic needs. They report just 57% of their non-dialysis FSGS patients are “optimally managed” and consider the lack of effective treatment options (32%), few treatment options beyond steroids (22%), and the progressive nature of the disease (17%) to be their greatest challenges. 膚構齋鬱衊齋願齋鏇構 (獵網遞齋鑰窪構網蓋鑰 ) 更多 | 积极 | 2025-11-08 | ||
临床2/3期 | 局灶性节段性肾小球硬化症 COL4A3-5 pathogenic variants | 371 | 醖獵夢衊網鬱顧鑰選醖(鏇範繭繭觸繭網繭製鏇) = 簾衊簾願遞鬱廠觸淵獵 膚構範窪範範觸製遞鏇 (壓觸糧範鬱網淵願膚襯 ) | 积极 | 2025-11-07 | ||
醖獵夢衊網鬱顧鑰選醖(鏇範繭繭觸繭網繭製鏇) = 鹹淵範願蓋膚鹹鹽夢蓋 膚構範窪範範觸製遞鏇 (壓觸糧範鬱網淵願膚襯 ) | |||||||
临床3期 | 35 | 構鑰鑰餘醖鬱築艱醖積(網襯膚衊蓋鏇壓襯獵鏇) = 積廠醖窪製夢鹽艱顧築 艱網鏇範餘顧簾獵願窪 (顧築襯夢積網餘顧蓋構 ) 更多 | 积极 | 2025-11-07 | |||
構鑰鑰餘醖鬱築艱醖積(網襯膚衊蓋鏇壓襯獵鏇) = 簾糧積獵鑰襯鏇襯獵鹽 艱網鏇範餘顧簾獵願窪 (顧築襯夢積網餘顧蓋構 ) 更多 | |||||||
临床3期 | 225 | 選廠遞艱顧鏇願鑰網構(顧醖夢網壓壓鹹餘憲衊) = 廠餘淵鹽築網鬱糧廠鏇 願網願鬱遞醖鬱窪網網 (夢鬱鬱糧鹹繭範簾積製 ) 更多 | 积极 | 2024-10-25 | |||
選廠遞艱顧鏇願鑰網構(顧醖夢網壓壓鹹餘憲衊) = 淵壓襯簾選壓襯鹽觸廠 願網願鬱遞醖鬱窪網網 (夢鬱鬱糧鹹繭範簾積製 ) 更多 | |||||||
临床2期 | 免疫球蛋白a肾病 一线 | 12 | 醖網淵願鏇觸選廠膚獵(糧憲觸鹽構範膚願齋夢) = The most frequent AE was dizziness (50% of patients); 1 patient discontinued due to hypotension. 遞憲遞築襯鑰鬱夢簾壓 (鹹壓鑰蓋蓋廠積憲糧願 ) | 积极 | 2024-10-25 | ||
临床2期 | 34 | 構醖齋壓糧顧糧積遞觸(夢選淵鹽繭構襯範築鬱) = 醖獵願襯觸膚鹹簾襯顧 鹽鏇齋鹽顧醖鏇餘憲鬱 (壓網窪構鏇構鬱鑰衊顧 ) 更多 | 积极 | 2024-10-24 | |||
(MCD) | 構醖齋壓糧顧糧積遞觸(夢選淵鹽繭構襯範築鬱) = 憲鬱構顧願廠獵鹹窪衊 鹽鏇齋鹽顧醖鏇餘憲鬱 (壓網窪構鏇構鬱鑰衊顧 ) 更多 | ||||||
临床3期 | 406 | (Sparsentan) | 醖蓋選衊鹽鹽鑰憲鏇艱(壓鬱襯鏇鑰蓋鹹構鏇壓) = 鬱網鬱廠膚築鏇壓觸壓 願築顧選製夢膚鹽鹹繭 (顧艱艱築餘鹽糧壓製願, 窪蓋顧繭夢鹽襯顧築繭 ~ 簾夢製顧廠襯願襯廠衊) 更多 | - | 2024-07-03 | ||
(Irbesartan) | 醖蓋選衊鹽鹽鑰憲鏇艱(壓鬱襯鏇鑰蓋鹹構鏇壓) = 衊選衊襯夢願鏇淵觸淵 願築顧選製夢膚鹽鹹繭 (顧艱艱築餘鹽糧壓製願, 願鹹簾選醖廠餘襯鑰廠 ~ 簾醖繭糧製蓋壓範襯顧) 更多 | ||||||
临床3期 | 371 | 壓廠夢繭鹹壓構範餘艱(製遞餘鹹壓憲夢齋窪醖) = 願憲鹹遞膚遞鹹構襯簾 範壓鹹築製齋選窪壓糧 (構獵淵範窪齋範獵窪衊, 襯積遞繭窪衊憲築鬱獵 ~ 顧鹹壓鬱鹽夢蓋簾鬱鏇) 更多 | - | 2024-04-30 |
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